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Stuart R. Stock

Researcher at Northwestern University

Publications -  182
Citations -  6757

Stuart R. Stock is an academic researcher from Northwestern University. The author has contributed to research in topics: Diffraction & Dentin. The author has an hindex of 40, co-authored 182 publications receiving 5943 citations. Previous affiliations of Stuart R. Stock include Argonne National Laboratory.

Papers
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Human Aortic Valve Calcification Is Associated With an Osteoblast Phenotype

TL;DR: These findings support the concept that aortic valve calcification is not a random degenerative process but an active regulated process associated with an osteoblast-like phenotype.
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Human degenerative valve disease is associated with up-regulation of low-density lipoprotein receptor-related protein 5 receptor-mediated bone formation.

TL;DR: The mechanism of valvular heart disease involves an endochondral bone process that is expressed as cartilage in the mitral valves and bone in the aortic valves and up-regulation of the Lrp5 pathway may play a role in the mechanism for valvULAR heart disease.
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Hyperelastic “bone”: A highly versatile, growth factor–free, osteoregenerative, scalable, and surgically friendly biomaterial

TL;DR: Hyperelastic “bone” did not elicit a negative immune response, became vascularized, quickly integrated with surrounding tissues, and rapidly ossified and supported new bone growth without the need for added biological factors, set it apart from many of the materials now available for bone repair.
Book

MicroComputed Tomography: Methodology and Applications

TL;DR: In this article, a back-projection Fourier-based reconstruction performance of micro-CT systems and their components has been evaluated using X-ray contrast and imaging images from the backprojection.
Journal ArticleDOI

Atorvastatin inhibits hypercholesterolemia-induced calcification in the aortic valves via the Lrp5 receptor pathway.

TL;DR: Hypercholesterolemic AV calcification is attenuated by atorvastatin and is mediated in part by the Lrp5/&bgr;-catenin pathway, which may be important in the signaling pathway of this disease.